Continued symptomatic improvement three to five years after transmyocardial revascularization with CO(2) laser: a late clinical follow-up of the Norwegian Randomized trial with transmyocardial revascularization.

OBJECTIVES: The goals of this study were to assess late clinical outcome and left ventricular ejection fraction (LVEF) after transmyocardial revascularization with CO(2) laser (TMR). BACKGROUND: During the 1990s TMR emerged as a treatment option for patients with refractory angina not eligible for conventional revascularization. Few reports exist on clinical effects and LVEF >3 years after TMR. METHODS: One hundred patients with refractory angina not eligible for conventional revascularization were block-randomized 1:1 to receive continued medical treatment or medical treatment combined with TMR. The patients were evaluated at baseline and after 3, 12 and 43 (range: 32 to 60) months with end points to angina, hospitalizations due to acute myocardial infarctions or unstable angina, heart failure and LVEF. Mortality was registered and MOS 36 Short-Form Health Survey answered at baseline and after 3, 6 and 12 months. RESULTS: Forty-three months after TMR, angina symptoms were still significantly improved, and unstable angina hospitalizations reduced by 55% (p < 0.001). Heart failure treatment (p < 0.01) increased, whereas the number of acute myocardial infarctions, LVEF and mortality was not affected. Quality of life was improved 3, 6 and 12 months after TMR. CONCLUSIONS: Forty-three months after TMR, angina symptoms and hospitalizations due to unstable angina were significantly reduced, heart failure treatment increased and LVEF and mortality were seemingly unaffected.

Experiences with citrate rather than heparin as an anticoagulant for ¹8F-FDG labeling of leukocytes.

UNLABELLED: In all reported clinical studies with (18)F-FDG-labeled leukocytes, heparin was used as an anticoagulant during labeling. Theoretically, the substitution of heparin with citrate should be advantageous. METHODS: Blood from healthy controls was sampled in duplicate, anticoagulated with citrate or heparin, and labeled with (18)F-FDG, and the labeling yield was measured. Viability was checked with the trypan blue exclusion technique. Moreover, 4 in vivo PET/CT studies were performed after the reinjection of leukocytes labeled after citrate anticoagulation. RESULTS: The labeling yields obtained with citrate and heparin were not significantly different (P = 0.447). Viability was greater than or equal to 99%. The quality of the PET/CT studies was excellent. In the in vivo studies, the mean labeling yield was 78%-better than or equal to that reported with heparin as an anticoagulant. CONCLUSION: Citrate is at least as effective as heparin as an anticoagulant, does not (unlike heparin) increase granulocyte activation, and should be the preferred anticoagulant for (18)F-FDG labeling of leukocytes.